Abstract

Abstract Developing tumors evade elimination by the immune system using a variety of mechanisms. Evidence suggests that cutaneous squamous cell carcinomas (cSCCs) may evade immune system surveillance by secreting complement factor H (CFH), a regulatory protein of the complement system. As part of its normal function, CFH binds to glycosaminoglycans on the surface of host cells where it acts as a cofactor for Factor I mediated C3b cleavage and accelerates the decay of the C3-convertase C3bBb. This mechanism for protecting self-cells also involves shifting the immune response from a pro-inflammatory T-helper-1 cell to an anti-inflammatory regulatory T-cell response. Data presented here suggest that some cSCCs have the ability to upregulate expression of CFH and studies have shown that this could be in response to the pro-inflammatory cytokine interferon-γ. We suggest that, in our cSCC samples, a potential negative-feedback loop exists in which the initial immune response to the developing tumor triggers expression of an immunosuppressive molecule, allowing the cancer to create an environment conducive to evading immune surveillance mechanisms. Note: This abstract was not presented at the meeting. Citation Format: Ellise Loomis, Christopher Pulford, Chandana Uppalapati, Agnes Pascual, McKale Montgomery, Kathryn J. Leyva, Elizabeth E. Hull. Cutaneous SCC may escape immune surveillance by secreting complement factor H [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr LB-181. doi:10.1158/1538-7445.AM2017-LB-181

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